Insulin's action on mammalian cells appears to be involved directly in the control of their fundamental biological functions, such as, glucose transport and utilization, activation of the biosynthesis pathways leading to fatty acid and protein synthesis, inhibition of free fatty acid mobilization by opposing depot fat lipase activity and promoting fatty acid esterification, etc. The current concept that insulin's "pleiotypic effects" on these regulatory processes are solely determined by glucose transport, is being seriously reconsidered in light of the findings that many important effects of insulin in the mammalian cells are also independent of D-glucose transport. This has led to the speculation that although the hormone reacts exclusively on the specific cell-surface receptors, it may generate a single or multiple messenger molecules to regulate the separate metabolic pathways within the cells. Attempts to identify any generalized messenger system have not yet been successful hitherto: Our aim is to recognize, isolate and characterize the reaction cycle within the plasma membrane which may be catalyzed by the hormone subsequent to its binding with the receptors and correlate these functions to the known loci of insulin-mediated reactions within the cells. Adipose cells are the most convenient model system for these studies. We believe that identification and characterization of the reactive plasma membrane components and of their product(s) may finally elucidate the mechanism of action of this hormone and the molecular changes leading to insulin-resistance.